The CC2D1A Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human K-562 cell line, engineered for loss-of-function studies of the CC2D1A gene. This knockout pool provides a heterogeneous population of edited cells, enabling robust functional screening and analysis without the bottleneck of single-cell cloning. The CRISPR/Cas9-mediated gene disruption targets CC2D1A, generating a versatile loss-of-function model for investigating its regulatory roles in signaling and trafficking.
K-562 is a widely used human chronic myelogenous leukemia (CML) cell line established from the pleural effusion of a 53-year-old female in blast crisis. These suspension cells harbor the BCR-ABL fusion oncogene, driving constitutive tyrosine kinase activity and aberrant proliferation. As a hematopoietic progenitor model, K-562 cells recapitulate key aspects of CML biology and serve as a standard platform for studying leukemogenesis, drug resistance, and signaling pathway alterations.
CC2D1A functions as a transcriptional repressor and negative regulator of NF-??B signaling, acting through direct interaction with IKK-?? (CHUK) to dampen expression of pro-inflammatory cytokines such as IL6 and TNF. It also represses transcription of serotonin receptor HTR1A and dopamine receptor DRD2 by binding cognate repressor elements. Additionally, CC2D1A participates in endosomal trafficking by engaging ESCRT complex components including HGS and STAM, linking receptor sorting to signal attenuation. Upstream activation by IKK-?? and stimulation by TNF-?? or TLR ligands converge on CC2D1A to modulate NF-??B p65/I??B-?? dynamics and endosomal cargo processing.
In the K-562 BCR-ABL-positive leukemia background, disruption of CC2D1A is expected to alter NF-??B pathway responsiveness and receptor trafficking dynamics. Given that NF-??B drives survival and proliferation signaling and that endosomal sorting influences receptor degradation and signal duration, CC2D1A knockout K-562 cells offer a unique tool to dissect how loss of this repressor affects leukemic cell behavior. Potential impacts include changes in cytokine output, sensitivity to kinase inhibitors, and modulations in the trafficking of growth factor or death receptors implicated in CML progression.
These polyclonal knockout cells are suited for a panel of downstream analyses, including RT-qPCR and RNA-seq for transcriptomic profiling, Western blotting and co-immunoprecipitation to verify disrupted protein interactions, and NF-??B luciferase reporter assays to quantify signaling activity. Researchers can employ flow cytometry to assess alterations in proliferation, apoptosis, or surface receptor expression. The population format supports high-throughput drug screening and CRISPR phenotyping without clonal bias. For additional information or ordering, please contact Ascent Research.
